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首页> 外文期刊>Pigment cell research >Sphingosylphosphorylcholine-induced ERK activation inhibits melanin synthesis in human melanocytes
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Sphingosylphosphorylcholine-induced ERK activation inhibits melanin synthesis in human melanocytes

机译：鞘氨醇磷酸胆碱诱导的ERK激活抑制人黑素细胞中黑色素的合成

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摘要

Sphingosylphosphorylcholine (SPC) is emerging as a potent signaling-lipid mediator. In this study, we investigated the effects of SPC on melanogenesis using cultured human melanocytes. Our results show that SPC significantly inhibits melanin synthesis in a concentration-dependent manner, and further that it reduces the activity of tyrosinase, the rate-limiting melanogenic enzyme. SPC treatment was also found to induce short-thick dendrites in human melanocytes, but not to reduce tyrosinase activity in a cell-free system, whereas kojic acid directly inhibited tyrosinase. These results suggest that SPC reduces pigmentation by indirectly regulating tyrosinase. In further experiments, SPC was found to downregulate microphthalmia-associated transcription factor (MITF) and tyrosinase, and Western blotting showed that SPC induces the activations of extracellular signal-regulated kinase (ERK) and 90 kDa ribosomal S6 kinase (RSK-1). Moreover, the specific ERK pathway inhibitor, PD98059, blocked the hypopigmentation effect of SPC, and abrogated the SPC-mediated downregulation of MITF. These results suggest that the ERK pathway is involved in the melanogenic signaling cascade, and that ERK activation by SPC reduces melanin synthesis via MITF downregulation.
机译：鞘氨醇磷酸胆碱（SPC）新兴作为有效的信号脂质介体。在这项研究中，我们调查了SPC使用培养的人黑素细胞对黑素生成的影响。我们的结果表明，SPC以浓度依赖性的方式显着抑制黑色素的合成，并且进一步降低了限速黑色素生成酶酪氨酸酶的活性。还发现，SPC处理可在人黑素细胞中诱导短厚度的树突，但在无细胞系统中不会降低酪氨酸酶活性，而曲酸可直接抑制酪氨酸酶。这些结果表明，SPC通过间接调节酪氨酸酶来减少色素沉着。在进一步的实验中，发现SPC下调小眼科相关转录因子（MITF）和酪氨酸酶，Western blotting显示SPC诱导细胞外信号调节激酶（ERK）和90 kDa核糖体S6激酶（RSK-1）的激活。此外，特异性ERK途径抑制剂PD98059阻止了SPC的色素沉着降低，并消除了SPC介导的MITF下调。这些结果表明，ERK途径参与了黑色素生成信号的级联反应，并且SPC激活ERK可以通过MITF下调降低黑色素的合成。

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